SHOCKING UPDATE! Statin drugs that lower cholesterol levels interfere with brain function and can induce symptoms interpreted as MS, ALS and Parkinson's Disease. It is also being shown that cholesterol levels have nothing to do with heart disease!! Dr Duane Graveline
Recently, the parmamafia have encouraged use of statins for MS, for the anti inflammatory effect.
It is madness to prescribe a drug FOR MS, that causes brain damage, and neurological symptoms!!
08/06/09
There was
a time when I believed that prescribed steroid treatments were beneficial,
and I attributed remission of symptoms to this drug. In clearer moments,
I recalled that I had recovered from several serious episodes, before and
after diagnosis, much faster, with NO drug therapy! After finding considerable
evidence in research that steroids have no positive effect on course of
ms, and many negative side effects, I ceased all drug therapy (1974).
We humans tend to
link observations to support our needs, and forget that just because two
things happen at the same time, does not mean they are necesarily related ....
Conflict of interest:
Readers need to be aware of the influence of financial support, sponsorship,
advertising ... most articles state possible conflict of interest. Is science
served by authors who design studies to support a position that has already
been decided?
Hans Selye warns
that experimental medicine is based upon the principle that, if a change
occurs only in those subjects receiving a certain treatment, then the treatment
must he regarded as the cause of the change. Here, the important fallacy
is that what you gave is not necessarily what acted. Errors in experimental
design or procedure, play some part in almost every fallacy,
Selye also warns
of dangerous traps in scientific reasoning, and how easy it is to miss
the discovery of what is clearly before us.
Articles I find interesting
...
Rasmnsky M and Sears
TA, Internodal Conduction in Undissected Demyelinated Nerve Fibres.
J Physiol(Lond) 227:323-350, 1972 - intracellular sodium
accumulation offered as
the explanation for (affected activity) seen in demyelinated fibres - position
of nodes inferred from assumption that nodes are the only
sites of inward membrane current - 3% of normal myelin sufficient for normal
function ..
em... steroids
affect the balance of sodium and potasium (mineralocorticoids) vital for
potential difference needed for signal transmission ...
Anat Achiron, Elon
Pras, R Gilad, Ilan Ziv, Mathilda Mandel, Carlos R Gordon, Shlomo Noy,
Ida Sarova-Pinhas & Eldad Melamed, Open Controlled Therapeutic Trial
of Intravenous Immune Globulin in Relapsing-Remitting Multiple Sclerosis.
Arch Neurol 49:1233-1236, 1992. During 12 month study
period immune globulin treated patients with MS improved by an average
of 0.3 Kurtzke units, while untreated control patients worsened
by 0.2 units. Improvement in the immune
globulin treated group, as well as the aggravation in the control group,
as compared with their scores before the treatment was
not statistically significant ... p 1235.
Nishihori T, Abdo-Matkiwsky
M , Fleishman SB, Blum RH, Severe action tremor related to interferon-alpha
2b therapy for
malignant melanoma. .Am J Clin Oncol. 2005 Oct;28(5):526.
Interferon (IFN)-alpha
2b is used for adjuvant therapy in malignant melanoma. Neurotoxicity
as a
side effect has been well described. Resting and action tremor related
to interferon have been
reported but are relatively uncommon. We report a case of a delayed-onset
interferon-related action
tremor in a patient with malignant melanoma.
Arne-Bes MC, [Neurotoxic
effects of medications: an update] [Article in French] Rev Med Liege. 2004;59
Suppl 1:118-23.
Unite des Maladies
Musculaires et Electrophysiologie, Service de Neurologie, Hopital Rangueil,
Toulouse. arne-bes.mc@chu-toulouse.fr
Peripheral neuropathy
is a common neurotoxic effect of medications. Antineoplastic agents
and antiretroviral medications
are most often involved: platinum compounds, vinca alkaloids,
taxols and nucleoside
reverse transcriptase inhibitors. These agents cause a dose-related
axonal polyneuropathy.
Symptoms are indicative of a predominantly sensory or sensory-motor
neuropathy which in some
cases is accompanied by dysfunction of autonomic nervous
system. Depending on dosage
and agent used symptoms resolve completely or not. Neurotoxic
effect can appear immediately
during or shortly after administration of the drug but sometimes
after cessation of chemotherapy.
In all cases the neuropathy alters the quality of life. A general
predisposition
for developing a neuropathy has been observed in nerves previously damaged
by diabetes mellitus, alcohol or in inherited neuropathy.
Within the past five years, some cases of
neuropathy
caused by alpha-interferon, statins or tacrolimus have
been reported. Although rare,
these aetiologies should be considered by physicians and the drugs removed
when others causes
of neuropathy have been excluded. Few cases of peripheral neuropathy have
been recently reported
with metronidazole, dapsone, nitrofurantoin or colchicin. Thalidomide
induces a dose-dependant
sensori-motor length-dependent axonal neuropathy(stiffness in legs-em).
It should be judiciously used
with close neurologic monitoring. Little is known about the mechanisms
responsible for the development
of neuropathy. Up to now, no drug is available to prevent or cure drug-induced
neuropathies.
Wichers MC, Koek
GH, Robaeys G, Verkerk R, Scharpe S, Maes M, IDO and interferon-alpha-induced
depressive symptoms: a
shift in hypothesis from tryptophan depletion to neurotoxicity. Mol Psychiatry.
2005 Jun;10(6):538-44. Department
of Psychiatry and Neuropsychology, Maastricht University, Maastricht, The
Netherlands. m.wichers@sp.unimaas.nl
Studies show that
administration of interferon (IFN)-alpha causes a significant increase
in depressive
symptoms. The enzyme indoleamine 2,3-dioxygenase (IDO), which converts
tryptophan (TRP) into
kynurenine (KYN) and which is stimulated by proinflammatory cytokines,
may be implicated in the
development of IFN-alpha-induced depressive symptoms, first by
decreasing the TRP availability
to the brain and second by the induction of the KYN pathway
resulting in the production
of neurotoxic metabolites.
Penny Whiting, Roger Harbord, Caroline
Main, Jonathan J Deeks, Graziella Filippini, Mathias Egger and Jonathan
AC Sterne,
Accuracy of magnetic
resonance imaging for the diagnosis of multiple sclerosis: systemic review,
British Medical Journal, 2006; 332: 875-8. f
... not
all patients who experience a first attack will develop the disease and
currently no treatment has been shown to delay
conversion to clinically definite multiple sclerosis or impact on long
term disability.
Valentine AD, Meyers CA, Neurobehavioral
effects of interferon therapy. Curr Psychiatry Rep, 2005
Oct;7(5):391-5.
... most common causes of treatment discontinuation
of Interferon (IFN) therapy ... associated with neuropsychiatric side
effects including cognitive dysfunction and mood syndromes of varying
severity ... approach 50% in recent studies. Effective management
of IFN-induced neuropsychiatric side effects should involve pretreatment
screening and interval assessment during therapy.
The
"re - discovery" of myelin repair in the year 2000, links repair of myelin
to chemical treatment.
The process of repair of myelin has been
proven spontaneous. When
we accept this fact, we can apply it to recovery. That’s my story.
June 2000 The
Boston Globe reports work claiming to be the first evidence of remyelination
...
Laurence M Howard, Amy J Miga,
Carol L Vanderluget, Mauro C Dal Canto, Jon D Laman, Randolph J Noelle
& Stephen D Miller (1999). J Clin Invest 103:281-290.
Mechanisms of immunotherapeutic intervention by anti-CD40L (CD154) antibody
in an animal model of multiple sclerosis. Supported
by US Public Health Service/National Institutes of Health Research grant
NS34819 (to S.D.Miller), NS30871 (to S.D.Miller), AI37075 (to R.J.Noelle),
and NS13011 (to M.C.Dal Canto), and by National Multiple Sclerosis Society
grants RG2275 (to S.D.Miller), RG2893 (to M.C.Dal Canto), and 5-38229 (to
R.J.Noelle).
REVIEW - by EM
Experimental subjects are mice immunized
with relapsing experimental autoimmune encephalitis (R-EAE)
[man made virus] to cause demyelination. Controls
were hamsters ...
Clinical signs of disease were evaluated
for up to 40 days ... by observation
Team members determined peak of acute
disease or remission ... by observation ...
mice were sacrificed 25 days after immunization
with anti-CD40L (CD154) antibody ... extensive areas of demyelination and
remyelination were observed. Authors
conclude that the repair of myelin was the result of the injections ...
June 2000 Los
Angeles Times reports that scientists repair MS-type damage for the first
time.
Researchers report that treating the
mice with the antibodies for five weeks caused myelin to re-grow.
Over that brief period, new myelin
repaired about 25 per cent of damaged areas.
Arthur E Warrington, Kunihiko
Asakura, Allan J Bieber, Bogoljub Ciric, Virginia Van Keulen, Srini V Kaveri,
Robert A Kyle, Larry R Pease & Moses Rodriguez, Proc Natl Acad Sci
7(12):6820-6825. (2000). Human monoclonal antibodies reactive to oligodendrocytes
promote remyelination in a model of multiple sclerosis. Supported
by National Institutes of Health Grant NS24180 and Acorda Therapeutics.
REVIEW - by EM
Mice 4-6 weeks old were injected with
Theiler's murine encephalomyelitis vaccine (TMEV)
resulting in plaque forming damage.
5 - 8 months later, animals
were given a single injection of human monoclonal antibodies (mAbs).
5 weeks after injection the animals were
sacrificed.
Area of remyelination in spinal cord sections
was estimated to be 47.7% in 10-12 spinal cord sections per
mouse, and 40.0% in all 32 sections. Estimated that new myelin
repaired about 25 per cent of damaged areas.
Authors conclude that treating the
mice with the antibodies caused myelin to re-grow ...
Review research on myelin repair:
JOURNAL REFERENCES
1 - Spontaneous repair of damaged myelin
begins in 17-19 days.
[This means that
myelin repair was underway long before injections began.]
2 - Movement speeds repair.
[Unrestrained animals
heal naturally.]
3 - Clinical condition is not related
to disease activity.
[Human observation
can not determine the peak of disease activity,
nor, when disease
activity ceases.]
Past research projects were designed
to study damage to myelin as it is observed
in multiple sclerosis, by using human
tissue in vitro, or post mortem tissue samples. These
studies using experimental animals, and normal controls, fixed tissue
samples for study at regular intervals, with the electron microscope. Spontaneous
repair of myelin was observed in mice (small mammals) in 1 week, and
in cats and rabbits (large mammals) in 7-31 days. Humans are classed as
large mammals. Many authors
have observed that thin repair is sufficient for resumption of normal function
in experimental animals, and, in humans.
One study (Bunge et al, 1961) observed
that the neurological condition of the experimental animal begins
to improve at a time when remyelination begins, and has returned to normal
by the time most axons are at least thinly
repaired.
Paul Freedman writes that society
honours the re-discoverer more than
the unexpected discoverer, not only
after the discovery has finally been
accepted, but more or less permanently. eg:
Rosslyn Franklin & DNA, PBS feature, Candace Pert & peptides, read
Molecules of Emotion)
In the New Millennium, we are ignoring
the discovery that is clearly behind us. Myelin
repairs itself! Repair is spontaneous & movement can speed healing
& recovery.